Method and apparatus for closed-loop stimulation of the hypoglossal nerve in human patients to treat obstructive sleep apnea

ABSTRACT

This invention is a fully implanted functional electrical stimulator ( 20 ) apparatus, a method for treatment of obstructive sleep apnea that provides for both reliable detection/prediction or airway occlusion that relieves, and/or prevents same by selective, direct electrical stimulation of the hypoglossal nerve (HG). The method, and apparatus sense hypoglossal nerve electro-neurogram activity for purposes of detecting or predicting obstructive sleep apnea. The sensed hypoglossal nerve activity, itself, is used to trigger functional electrical stimulation of the hypoglossal nerve in order to improve upper airway patency. Further, an improved hypoglossal nerve stimulation electrode ( 10 ) interface (IC) is provided that allows for simultaneous hypoglossal nerve activity sensing, and stimulation by eliminating stimulation artifacts that would otherwise trigger further erroneous stimulation.

CROSS-REFERENCE TO RELATED APPLICATION

This application claims the benefit of the filing date of internationalapplication no. PCT/US99/16913 having an international filing date ofJul. 27, 1999 which claims priority from U.S. provisional applicationNo. 60/094,263 filed Jul. 27, 1998.

BACKGROUND OF THE INVENTION

The present invention relates generally to the functional electricalstimulation (FES) arts. More particularly, the present invention relatesto a method and apparatus for sensing hypoglossal nerve activity inhuman patients to detect obstructive sleep apnea, and using the sensedhypoglossal nerve activity to trigger selective functional electricalstimulation of the hypoglossal nerve, itself, for purposes of improvingupper airway patency and, thus, treating obstructive sleep apnea.Further, the present invention relates to an improved hypoglossal nervestimulation electrode interface that allows for simultaneous hypoglossalnerve activity sensing and nerve stimulation by eliminating stimulationartifacts that would otherwise trigger further, erroneous stimulation.

Obstructive sleep apnea (OSA) is the recurrent occlusion of the upperairways of human patients during sleep. In these patients, the upperairways obstruct as often as several times a minute with each episodelasting as long as 20-30 seconds. Each apneic episode ends with a briefarousal from sleep. Consequently, arterial oxyhemoglobin saturationdecreases drastically. Complications include excessive daytimesleepiness, restless sleep, morning headache, job-related accidents,impaired short-term memory, polycythema, hypertension, right-sidedcongestive heart failure, decreased libido, and the like. Personalitydisorder and other psychological problems may also develop over time.Obstructive sleep apnea is found in 2 to 4 percent of the population,primarily in adult men and post-menopausal women.

In humans, the hypoglossal nerve innervates the intrinsic and extrinsicmuscles of the tongue and the geniohyoid muscle. Of these musclesinnervated by the hypoglossal nerve, the genioglossus and the geniohyoidmuscles are the primary muscles involved in dilating the upper airways(UAWS) . Contraction of the genioglossus muscle provides tongueprotrusion and, hence, dilates the airways.

It is generally known that the flow of inspired air is doubled bystimulation of the main branch of the hypoglossal nerve. Stimulation ofthe medial branch was nearly as effective and was superior tostimulation of other branches. Attempts have been made to improve upperairway patency in humans during sleep via direct electrical stimulationof the hypoglossal nerve. Further, various physiological variables havebeen used to synchronize the electrical stimulation with respiration.Hypopharyngeal or espophageal pressure measurements, airflowmeasurements made with thermistors placed near the nose and mouth, andtracheal inter-ring distance measurements made with a strain gauge areexamples of physiological variables that have been investigated for usein synchronization of electrical stimulation of the hypoglossal nerveand/or the genioglossus muscle. However, all of these methods havedrawbacks and limitations.

Other treatment methods for obstructive sleep apnea have included use ofa nose mask through which continuous positive airway pressure is appliedto keep the upper airways open. This therapy must be continuedindefinitely, and only 60-65 percent of these patients can tolerate thetechnique long-term. Tracheostomy is another treatment for severeobstructive sleep apnea, but it is rarely used because of low patientacceptability and relatively high morbidity. Uvulopalatopharyngoplasty,removal of redundant tissue in the oropharynx, and other surgicaloperations to correct anatomical abnormalities in the upper airways canbe considered in certain cases. However, in general, all of theabove-mentioned therapies are associated with complications anddisadvantages. Weight loss may improve the condition in mild cases, butpharmacologic attempts to treat obstructive sleep apnea by increasingpharyngeal muscle activity during sleep have not been found to beeffective. Presently, electrical stimulation of the tongue muscles isthe only known alternative treatment method that may provide somebenefits.

In light of the foregoing, there has been found a need for a fullyimplantable functional electrical stimulator apparatus and method fortreatment of obstructive sleep apnea that provides for both reliabledetection of airway occlusion and that relieves same by selectiveelectrical stimulation of the hypoglossal nerve. Further, a need hasbeen identified for such a method and apparatus that accomplishes theseresults without relying upon use of external (i.e., non-implanted)devices that require percutaneous and/or transcutaneous interfaces andwithout requiring use of multiple, separate electrodes and sensors.Also, it has been deemed necessary to provide a method and apparatus forsimultaneously sensing hypoglossal nerve activity and for using thesensed hypoglossal nerve activity to trigger selective electricalstimulation of the hypoglossal nerve without erroneously triggeringfurther stimulation due to stimulation artifacts.

SUMMARY OF THE INVENTION

In accordance with the present invention, a new method and apparatus areprovided for treating obstructive sleep apnea in humans by way ofclosed-loop electrical stimulation of the hypoglossal nerve, whereinactivity of the hypoglossal nerve, itself, triggers the electricalstimulation.

In accordance with a first aspect of the present invention, a method oftreating obstructive sleep apnea in a human patient comprises monitoringthe patient for occlusion of his/her upper airways associated withobstructive sleep apnea by sensing electroneurogram activity of thepatient's hypoglossal nerve. The hypoglossal nerve of the patient isdirectly electrically stimulated when occlusion of the upper airwaysoccurs as indicated by the sensed electroneurogram activity of thehypoglossal nerve.

In accordance with a more limited aspect of the invention, theelectroneurogram signal of the patient's hypoglossal nerve, itself, isused to trigger the direct electrical stimulation of the hypoglossalnerve.

In accordance with another aspect of the present invention, an apparatusfor treatment of obstructive sleep apnea comprises means for detectingat least partial occlusion of upper airways of a human patient bysensing electroneurogram activity of a hypoglossal nerve of the patient.Means are provided for directly electrically stimulating the hypoglossalnerve of the patient in response to at least partial occlusion of theupper airways of the patient as indicated by the detecting means.

In accordance with still another aspect of the present invention, anapparatus adapted for simultaneously electrically stimulating bodytissue and monitoring electrical activity of the body tissue beingelectrically stimulated without stimulation artifact is defined. Theapparatus includes an electrical stimulation source and a sensor incontact with body tissue. A first stimulation contact is also in contactwith the body tissue, and the said body tissue defines an electricalpath between the first stimulation contact and the sensor having a firstelectrical impedance. A second stimulation contact is also in contactwith the body tissue, and the body tissue defines an electrical pathbetween the second stimulation contact and the sensor that has a secondelectrical impedance. The first impedance is substantially equal to thesecond impedance. A trigger receives input from the sensor andselectively triggers electrical stimulation of the body tissue by thestimulation source so that at least one electrical pulse passes betweenthe first and second stimulation contacts through the body tissue.During stimulation, the potential difference established between thefirst stimulation contact and the sensor in response to the electricalpulse is substantially equal in magnitude to the potential differenceestablished between the second stimulation contact and the sensor.

One advantage of the present invention resides in the provision of amethod and apparatus for closed-loop stimulation of the hypoglossalnerve in a human to treat obstructive sleep apnea.

Another advantage of the present invention is found in the provision ofa method and apparatus for treatment of obstructive sleep apnea whereinhypoglossal nerve activity is sensed and used to determine when upperairway occlusion associated with obstructive sleep apnea is occurring.

Still another advantage of the present invention is the provision of amethod and apparatus for stimulation of the hypoglossal nerve inobstructive sleep apnea patients wherein sensed activity of thehypoglossal nerve in the patient triggers electrical stimulation of thehypoglossal nerve when the sensed activity of the hypoglossal nerve isindicative of occlusion of the patient's upper airways so that theocclusion is prevented or removed.

A further advantage of the present invention is the provision of amethod and apparatus for closed-loop stimulation of the hypoglossalnerve in obstructive sleep apnea patients wherein hypoglossal nerveactivity is sensed simultaneously with stimulation of the hypoglossalnerve.

Still another advantage of the present invention resides in theprovision of an apparatus for treatment of obstructive sleep apnea inhuman patients wherein the apparatus is totally implantable in thepatient and requires no external devices or percutaneous electricalleads.

A yet further advantage of the present invention is found in theprovision of a method and apparatus for closed-loop stimulation of thehypoglossal nerve in human patients for purposes of treating obstructivesleep apnea wherein a single, multiple-contact (i.e., >1 contact)electrode is implanted in the patient for sensing/stimulation ratherthan multiple, separate electrodes/sensors.

A still further advantage of the present invention resides in theprovision of a method and apparatus for treatment of obstructive sleepapnea wherein the onset of obstructive sleep apnea is predicted so thatit can be prevented before it becomes severe.

Still other benefits and advantages of the present invention will becomeapparent to those of ordinary skill in the art to which the inventionpertains upon reading and understanding the specification andaccompanying drawings.

BRIEF DESCRIPTION OF THE DRAWINGS

The invention takes form in certain components and arrangements ofcomponents, and in certain steps and arrangements of steps, preferredembodiments of which are described herein and illustrated in theaccompanying drawings that form a part hereof and wherein:

FIG. 1 is a block diagram illustrating a system used for recordinghypoglossal nerve activity and for closed-loop stimulation of thehypoglossal nerve;

FIG. 2 graphically illustrates hypoglossal nerve response when airwayocclusion was caused by application of force;

FIG. 3 graphically illustrates closed-loop stimulation of thehypoglossal nerve during NREM sleep using electroneurogram activity ofthe hypoglossal nerve, itself, to trigger the electrical stimulation;

FIG. 4 graphically illustrates esophageal pressure under normalconditions, airway occlusion, and hypoglossal nerve electricalstimulation during airway occlusion;

FIG. 5 is a diagrammatic illustration of a closed-loop system forstimulation of the hypoglossal nerve for treatment of obstructive sleepapnea in accordance with a preferred embodiment of the presentinvention; and,

FIG. 6 is a schematic diagram of an electrode/sensor interface circuitformed in accordance with the present invention and adapted forclosed-loop stimulation of the hypoglossal nerve of a human patient fortreatment of obstructive sleep apnea wherein stimulation artifacts areeliminated from the sensing circuit to prevent erroneous stimulation inresponse to the artifacts.

DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS

Referring now to the drawings, wherein the showings are for purposes ofdescribing preferred embodiments of the invention only and not forpurposes of limiting same, a closed-loop method and apparatus forclosed-loop stimulation of the hypoglossal nerve in human patients totreat obstructive sleep apnea is described. Heretofore, there has beeninsufficient understanding of the role of the hypoglossal nerve inobstructive sleep apnea and, consequently, there has not been provided amethod and apparatus for treatment of obstructive sleep apnea bystimulation of the hypoglossal nerve wherein activity of the hypoglossalnerve is used to detect airway obstruction. Accordingly, FIGS. 1-4relate to the development of the present invention through study ofvarious dogs. Those of ordinary skill in the art will appreciate thatthe information set forth in FIGS. 1-4 and the accompanying text of thedisclosure has application to human patients, as well.

Referring to FIG. 1, an apparatus for studying the role of thehypoglossal nerve in obstructive sleep apnea and treatment of same isillustrated. Two healthy Beagles with normal upper airway anatomy werechronically implanted with spiral nerve cuff electrodes 10 on the maintrunk of the hypoglossal nerve HG, and electroencephalogram (EEG) andelectro-oculogram (EOG) electrodes (not shown) on the skull for sleepstaging in the same surgical procedure. The cuff electrode 10 used forthe present study were 20 millimeters (mm) in length and 2.5 mm indiameter, with first, second, and third contacts 10 a,10 b,10 c, andwere implanted bilaterally in one animal (Beagle#1) and unilaterally inthe other (Beagle#2).

A custom-design apparatus that does not form part of the presentinvention was used to apply force selectively on the submental region ofthe dogs, approximately a few centimeters rostral to the hyoid bone, forpurposes simulating occlusion of the upper airways in the dogs as wouldoccur during obstructive sleep apnea in human patients. A custom-madecylindrical balloon, also not forming a part of the present invention,was placed inside the animal's esophagus before each sleep session formeasurements of the esophageal pressure (Pes) Respiratory abdominalmovements ABD (FIG. 2) of each dogs were measured with a plethysmographthat had an inductive band transducer worn around the belly. All the rawsignals were continuously digitized by a digital data recorder 14, suchas a Digital Data Recorder Model VR-10B available commercially fromInstrutech Corp., New York. The raw data signals were also and stored onvideo tapes by a video tape recorder 16 during sleep sessions.

With the two dogs studied, a total of 53 sleep sessions were held spreadover a period of 17 months. Each session lasted between 2-4 hours andincluded multiple sleep cycles. Non-Rapid Eye Movement (NREM) sleepstage was characterized with larger amplitudes and slower frequencycomponents in the EEG signal relative to either wakefulness or Rapid EyeMovement (REM) sleep stage. The maximum submental force applied usingthe force applicator was defined as the largest force value at which theanimal was not aroused from sleep.

Hypoglossal nerve HG stimulation was by a conventional pulse trainstimulator 20, such as a Grass S88 stimulator available commerciallyfrom Grass Medical Instruments, at the maximum submental force level insome of the sessions using either manual triggering via switch 22 in thebeginning of each breath or in a closed-loop manner using activity ofthe hypoglossal nerve HG, itself, as the trigger with the switch 22 inposition “1.” Here, at this early stage of the study, false triggers dueto stimulation artifacts in the electroneurogram signal of thehypoglossal nerve HG as recorded by the recorder 14 were prevented bydisabling the output of the trigger enabling circuit 24 for about aninter-breath interval.

Electrical stimulation from the stimulator 20 was applied to thehypoglossal nerve HG between the second (middle) contact lob and thefirst and third (end) contacts 10 a,10 c of the tripolar cuff electrode10 through an optically isolated voltage to current converter unit 30. Atrain of cathodic pulses with a train duration of 1-3 seconds at a pulsefrequency of approximately 40 Hz, pulse width of 100 microseconds (μS)and at pulse amplitudes between 0.2 to 0.6 milliamps (mA) were used. Tenbreaths during and ten breaths between the stimulated breaths wereallowed before raising the current amplitude to a higher value.

The hypoglossal nerve electroneurogram signal HGS was amplified andfiltered between 300 Hertz (Hz) and 10 Kilohertz (kHz) by amplifier 36such as a P5 Series amplifier also available commercially from GrassMedical Instruments resulting in the signal HGS'. Theelectroencephalogram and EOG signals (not shown) were band-pass filteredbetween 1 Hz to 30 Hz. The pressure measurements from the submentalforce applicator and the esophageal balloon were amplified withcustom-made DC amplifiers (not shown). The amplified signal HGS' fromthe hypoglossal nerve HG was digitized and converted to an appropriateformat for storing on video tapes at a rate of 47.2 kilosamples/secondby the digital data recorder 14. Other raw signals were digitized at arate of 60 sample/s.

The recordings of the amplified hypoglossal nerve signal HGS' werefurther filtered with a custom design band-pass filter 38. The band-passfilter 38 comprised a third order high pass Butterworth filter at 900 Hzand a second order low pass Butterworth filter at 2400 Hz to eliminateelectromyogram (EMG) contamination from the nearby muscles and passedthrough a rectifier and 100 millisecond (ms) time averager 40, and athreshold detector 42 to produce the trigger signal TS for electricalstimulation of the hypoglossal nerve HG via stimulator 20.

For frequency spectrum analysis, the raw hypoglossal nerve signals HGS'were replayed from the video tapes and resampled at a rate of 20,000samples/second using a data acquisition board 44 and a programmedgeneral purpose computer PC. For breath-by-breath analysis and thetemporal plots of the data, the rectified and averaged version of thehypoglossal nerve signal HGS' and other measured variables were sampledat a rate of 60 sample/second into the computer PC. The area under theesophageal pressure trace during the inspiratory time (AreaPes) wascalculated in each breath to evaluate the effect of loading andelectrical stimulation on the size of the upper airway passage.

Recordings of the hypoglossal nerve signal HGS' had a phasic componentabove a baseline when the upper airways in the dogs were loaded with thesubmental force in NREM sleep to cause occlusion of the airways. Thephasic activity of the hypoglossal nerve signal HGS' increasedimmediately in the following breath as a response to an increase in thesubmental force and stayed at an elevated activity level as long as theforce was applied as illustrated in FIG. 2.

The mean signal-to-noise ratio in the hypoglossal nerve signal HGS',defined as the peak phasic activity divided by the baseline in signalafter it has been rectified and averaged by the rectifier/averager 40,had a mean±standard deviation of 2.37±0.74 (n=25 force maneuvers) at themaximum submental force level. The hypoglossal nerve HG was active inevery breath cycle at the maximum submental force level. Airflow-limitedinspiration was often observed at the maximum force as confirmed by thepresence of snoring. The esophageal pressure Pes also increased withapplication of the submental force. The correlation between the area ofphasic hypoglossal nerve HG activity and AreaPes, was R=0.82 and R=0.88for the two dogs, respectively. The onset time of the phasic hypoglossalnerve HG activity with respect to the beginning of the phasic esophagealpressure was measured at the maximum force level on breath-by-breathbasis in multiple trials. The phasic hypoglossal nerve signal HGS' beganto rise earlier than the esophageal pressure with a mean+standarddeviation onset time of 17±196 ms (220 breaths in 20 force maneuvers).

FIG. 3 demonstrates closed-loop stimulation of the hypoglossal nerveusing its own electroneurogram activity as the feedback signal. Thesubmental force to cause airway occlusion was first raised to 6 N toload the upper airways. As a result, the phasic components of thesubmental force and the hypoglossal nerve activity signal HGS'increased. The closed-loop operation was started at time≡110 seconds. Inthis (and all other) stimulation trial(s), the threshold for triggeringstimulation of the hypoglossal nerve in the activity signal HGS was setjust above the baseline of same. At the start of each breath, theelectronic circuitry detected the onset of the phasic hypoglossal nerveactivity signal HGS' and triggered the stimulator 20 that, in turn,generated a train of pulses (pulse width=100 μs at 40 Hz) for apredetermined period of time (3s). Upon detection of each phasiccomponent of the activity signal HGS', the output of the trigger enablecircuit 24 was disabled for approximately one inter-breath interval (5s) to prevent false stimulation of the nerve due to the stimulationartifacts in the nerve activity signal HGS'. Using the system of FIG. 1,the phasic bursts of the activity signal HGS' were completely obscuredby the stimulation artifacts in the recordings since the detectionoccurred very early in each breath cycle. The animal took a deeperbreath on the first stimulated breath indicating a relief from theeffect of the submental force. The amplitude of the phasic esophagealpressure (Pes) stayed at a low level as long as the electricalstimulation (Stim) was applied and returned to its pre-stimulation levelwithin the next breath at the end of the stimulation. The EEG channelindicated no arousal from sleep during stimulation.

The effect of the electrical stimulation on the area of the phasicesophageal pressure (AreaPes) in NREM sleep is shown in FIG. 4. Thesubmental force value of 0 Newtons (N), representing no airwayocclusion, was applied as control. A submental force application valueof 5 N caused airway occlusion and a 2 to 3 fold increase in AreaPes.Direct electrical stimulation of the hypoglossal nerve HG at 0.2 mA didnot result in significant large changes in the pressure measurements.However, AreaPes fell rather sharply with increasing current amplitudesof the stimulus pulse train (Stim) and it returned to near controlvalues indicating a complete removal of the upper airway occlusioneffect caused by the submental force application. In these trials, theanimal was not aroused from sleep even at a current amplitudes 50%larger than what was sufficient to completely reverse the loading effectof the submental force (0.6 mA vs. 0.4 mA).

The foregoing shows the feasibility of the closed-loop stimulation ofthe hypoglossal nerve HG using it's activity HGS,HGS' as the feedbacksignal. The hypoglossal nerve signal recordings obtained with cuffelectrodes 10 have sufficiently large signal-to-noise ratios fordetection of the phasic component without missing a breath when theairways are loaded with the maximum force. Conventional filteringtechniques and algorithms are adequate to prevent false detections dueto baseline shifts and electromyogram (EMG) contamination from thesurrounding muscles. The hypoglossal nerve signal HGS' recorded in thisstudy is thought to be primarily of efferent origin since the afferentfibers in the hypoglossal nerve HG are few in number.

FIG. 5 diagrammatically illustrates a preferred embodiment of anapparatus for closed-loop stimulation of the hypoglossal nerve HG inhuman patients to treat obstructive sleep apnea. The apparatusillustrated in FIG. 5 is similar to that illustrated in FIG. 1 and isadapted for connection to the tri-polar nerve cuff electrode 10including first, second, and third contacts 10 a,10 b,10 c adapted forconnection about the hypoglossal nerve HG of the patient being treatedand connected to an electrode interface circuit IC via first, second,and third leads 11 a,11 b,11 c, respectively. The electrode 10 acts asboth hypoglossal nerve stimulation electrode and a hypoglossal nerveactivity sensor as described in full detail below. The apparatusillustrated in FIG. 5 is adapted for total implantation in the patientbeing treated without the need for associated external components. Thoseof ordinary skill in the art will recognize that electrodes other thanthe illustrated tri-polar electrode may be used without departing fromthe overall scope and intent of the present invention. It is notintended that the invention be limited to any particular type ofelectrode.

The interface circuit IC receives hypoglossal nerve electroneurogramactivity input from the electrode 10 and supplies a hypoglossal nerveactivity signal HGS to the amplifier 36. The amplifier 36, described indetail above in relation to FIG. 1, supplies an amplified and filteredhypoglossal nerve activity signal HGS' to a signal conditioning andalgorithm circuit 50 that comprises the band-pass filter 38, therectifier and averager 40, and the threshold detector 42 describedabove. When the threshold detector 42 of the signal conditioning andalgorithm circuit 50 detects at least partial occlusion of the patient'supper airways by corresponding hypoglossal nerve activity above a selectthreshold as indicated by the amplified/filtered signal HGS', it outputsa trigger signal TS to the stimulator 20. When the stimulator 20receives the trigger signal TS, it outputs a stimulation pulse train(Stim) to the hypoglossal nerve HG by way of the interface circuit ICand electrode 10 to lessen the airway occlusion and prevent obstructivesleep apnea. Preferably, in the closed-loop system, the stimulator 20 istriggered to output the stimulation pulse train (Stim) wheneverelectroneurogram activity of the hypoglossal nerve HG is above a selectthreshold over the baseline, i.e., when electroneurogram activity of thehypoglossal nerve HG exceeds the baseline activity experienced when noocclusion of the upper airways is present by a select amount. Of course,the baseline activity for a particular patient cannot be determineduntil the closed-loop stimulation apparatus is implanted and tested.

Operation of the interface circuit IC is best understood with referencealso to FIG. 6. In general, the electrode is connected to the interfacecircuit IC so that the first and third electrode contacts 10 a,10 c actas stimulation contacts and so that the central, second contact 10 bacts as a hypoglossal nerve electroneurogram activity sensor. Theinterface circuit IC has been found to be highly desirable because, asdescribed herein, it suppresses electromyogram (EMG) signals frommuscles surrounding the hypoglossal nerve HG to prevent these signalsfrom interfering with accurate sensing of hypoglossal nerve activity.Further, the interface circuit IC suppresses stimulation artifacts inthe hypoglossal nerve activity signal HGS due to application of thestimulation pulse train (Stim) by the stimulator 20.

More particularly, as illustrated in FIG. 8, the interface circuit ICcomprises a transformer TR1 including first, second, and third inductorcoils L1,L2,L3, and further comprises a variable resistor such as thepotentiometer R1. The amplifier 36 is connected to first and secondoutput terminals AMP1,AMP2. The stimulator 20 is connected to theinterface circuit IC by way of first and second input terminalsSTIM1,STIM2 so as to be connected across the coil L3 of the transformerTR1. The transformer TR1 is designed to operate at the frequency of thestimulation pulse train input signal (Stim), and the coils L1,L2,L3 ofthe transformer are very tightly coupled to minimize stray inductances.The reactive impedances of the “magnetizing coils” are also very high inthe input signal (Stim) operating frequency range. Those of ordinaryskill in the art will recognize that the transformer TR1 need not belarge because the energy transferred thereby is only several milliwatts.

In operation, when the stimulation input signal (Stim) is input to theinterface circuit IC, the voltage induced across the coil L3 by thecurrent IL3 is also induced across the coils L1,L2 of a like amplitude(n1=n2) by the currents IL1,IL2. This, then causes stimulation of thehypoglossal nerve HG by a current IL1,IL2 that flows through a circuitcomprising the coils L1,L2, the third contact 10 c, the tissue of thehypoglossal nerve HG, and the first electrode contact 10 a. Thestimulation artifact is canceled from the hypoglossal nerve activitysignal HGS due to the fact that the sensing contact 10 b divides theimpedance between the first and third contacts 10 a,10 c equally. Thus,the bridge consisting of the tissue of the hypoglossal nerve HG and thetransformer TR1 is balanced so that, upon stimulation of the nerve HG,no potential difference is present at the first and second outputterminals AMP1,AMP2 connected to the amplifier 36. On the other hand,pure hypoglossal nerve electroneurogram activity, itself, will cause apotential difference at the terminals AMP1,AMP2 and cause amplificationof the signal HGS that is then fed to the signal conditioning andalgorithm circuit 50 as described above. If necessary, the potentiometerR1 can be adjusted after the device is implanted to ensure that thebridge is balanced and the stimulation artifact canceled. Furthermore,undesirable electromyogram (EMG) activity received through the first andthird contacts 10 a,10 c is also canceled out due to the symmetricalarrangement of the contacts 10 a,10 c and the coils L1,L2.

In light of the foregoing, those of ordinary skill in the art willrecognize that the present invention provides a method and apparatus forusing electroneurogram activity of the hypoglossal nerve to detectocclusion of the upper airways in a human patient, and for using theelectroneurogram signal sensed from the hypoglossal nerve to triggerdirect electrical stimulation of the hypoglossal nerve to remove theairway occlusion.

The invention has been described with reference to preferredembodiments. Obviously, modifications and alterations will occur toothers upon reading and understanding the preceding specification. It isintended that the invention be construed as including all suchmodifications and alterations insofar as they are within the scope ofthe appended claims and equivalents thereto.

Having described the preferred embodiments, the invention is claimed tobe:
 1. A method of treating obstructive sleep apnea in a human patient,said method comprising: monitoring said human patient for at leastpartial occlusion of upper airways of said patient associated withobstructive sleep apnea by sensing electroneurogram activity of ahypoglossal nerve of the patient; and, directly electrically stimulatingthe hypoglossal nerve of the patient when at least partial occlusion ofthe upper airways of the patient occurs as indicated by said sensedelectroneurogram activity of said hypoglossal nerve.
 2. The method oftreating obstructive sleep apnea as set forth in claim 1 wherein saidstep of monitoring said human patient for occlusion of the upper airwayscomprises: identifying at least partial occlusion of the upper airwaysof the patient when said sensed hypoglossal nerve electroneurogramactivity rises above a baseline electroneurogram activity level of saidhypoglossal nerve by a select amount, said baseline electroneurogramlevel corresponding to a level of electroneurogram activity of saidhypoglossal nerve present when said upper airways of said patient arenot at least partially occluded.
 3. The method of treating obstructivesleep apnea as set forth in claim 1 further comprising: amplifying saidsensed electroneurogram activity of said hypoglossal nerve to obtain anamplified electroneurogram signal; and, using said amplifiedelectroneurogram signal to trigger said direct electrical stimulation ofsaid hypoglossal nerve.
 4. The method of treating obstructive sleepapnea as set forth in claim 1 wherein stimulating the hypoglossal nerveof the patient is accomplished with a train of stimulus pulses eachhaving an amplitude of greater than 0.2 mA.
 5. The method of treatingobstructive sleep apnea as set forth in claim 1 wherein said step ofdirectly electrically stimulating said hypoglossal nerve comprises:connecting a nerve electrode to said hypoglossal nerve so that saidnerve electrode at least partially encircles said hypoglossal nerve; andpassing electrical stimulation pulses between first and second contactsof said nerve electrode through tissue of said hypoglossal nerve.
 6. Themethod of treating obstructive sleep apnea as set forth in claim 5wherein said step of monitoring said human patient for at least partialocclusion of the upper airways by sensing electroneurogram activity ofsaid hypoglossal nerve comprises: sensing electroneurogram activity ofsaid hypoglossal nerve with a third contact of said nerve electrode,said third contact arranged relative to said first and second contactsso that a first impedance defined between said first contact and saidthird contact through said tissue of said hypoglossal nerve issubstantially equal to a second impedance defined between said secondcontact and said third contact through said tissue of said hypoglossalnerve.
 7. An apparatus for treatment of obstructive sleep apnea in ahuman patient, said apparatus comprising: means for detecting at leastpartial occlusion of upper airways of said human patient by sensingelectroneurogram activity of a hypoglossal nerve of the patient; and,means for directly electrically stimulating the hypoglossal nerve of thepatient in response to at least partial occlusion of the upper airwaysof the patient as indicated by said means for detecting at least partialairway occlusion.
 8. The apparatus for treatment of obstructive sleepapnea as set forth in claim 7 wherein said means for detecting at leastpartial airway occlusion detects at least partial occlusion of the upperairways of the patient when said sensed hypoglossal nerveelectroneurogram activity rises above a baseline electroneurogramactivity level of said hypoglossal nerve by a select amount, saidbaseline electroneurogram level corresponding to a level ofelectroneurogram activity of said hypoglossal nerve present when saidupper airways of said patient are not at least partially occluded. 9.The apparatus as set forth in claim 7 further comprising: means foramplifying said sensed electroneurogram activity of said hypoglossalnerve to obtain an amplified electroneurogram signal; and, trigger meansfor receiving said amplified electroneurogram signal and triggering saiddirect electrical stimulation of said hypoglossal nerve when saidamplified signal exceeds a baseline activity level of said signal by aselect amount.
 10. The apparatus as set forth in claim 7, wherein saidmeans for electrically stimulating the ypoglossal nerve of the patientstimulates the hypoglossal nerve with a train of stimulus pulses eachhaving an amplitude of greater than 0.2 mA.
 11. The apparatus as setforth in claim 7 further comprising: a nerve electrode having twocontacts, said electrode adapted to be connected to and at leastpartially encircling said hypoglossal nerve, wherein said means forelectrically stimulating said hypoglossal nerve passes electricalstimulation pulses between said first and second contacts of said nerveelectrode through tissue of said hypoglossal nerve.
 12. The apparatus asset forth in claim 11 further comprising a third contact on saidelectrode, wherein said means for detecting at least partial occlusionof said patient's airways senses electroneurogram activity of saidhypoglossal nerve with said third contact of said nerve electrode, saidthird contact arranged relative to said first and second contacts sothat a first impedance defined between said first contact and said thirdcontact through said tissue of said hypoglossal nerve is substantiallyequal to a second impedance defined between said second contact and saidthird contact through said tissue of said hypoglossal nerve.